Case ReportAntineutrophil Cytoplasmic Antibody Induction due toInfection: A Patient with Infective Endocarditis and ChronicHepatitis C

Fareed B. Kamar1 and T. Lee-Ann Hawkins2

1Department of Medicine, University of Calgary, Calgary, AB, Canada T2N 4N12Department of Medicine, Division of General Internal Medicine, University of Calgary, Calgary, AB, Canada T2N 4N1

Correspondence should be addressed to Fareed B. Kamar; fbkamar@ucalgary.ca

Received 10 June 2015; Accepted 21 December 2015

Copyright © 2016 F. B. Kamar and T. L.-A. Hawkins. This is an open access article distributed under the Creative CommonsAttribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work isproperly cited.

While antineutrophil cytoplasmic antibody (ANCA) is often used as a diagnostic marker for certain vasculitides, ANCA inductionin the setting of infection is much less common. In the case of infective endocarditis, patients may present with multisystemdisturbances resembling an autoimmune process, cases that may be rendered even trickier to diagnose in the face of a positiveANCA. Though not always straightforward, distinguishing an infective from an inflammatory process is pivotal in order to guideappropriate therapy. We describe an encounter with a 43-year-old male with chronically untreated hepatitis C virus infection whofeatured ANCA positivity while hospitalized with acute bacterial endocarditis. His case serves as a reminder of two of the fewinfections known to uncommonly generate ANCA positivity. We also summarize previously reported cases of ANCA positivity inthe context of endocarditis and hepatitis C infections.

1. Introduction

The antineutrophil cytoplasmic antibody (ANCA) class ofimmunoglobulins features the principal subtypes c-ANCAand p-ANCA, which are predominantly generated against thecytosolic antigens proteinase 3 (PR3) and myeloperoxidase(MPO), respectively [1].The presence of these autoantibodieshas been described in a variety of autoimmune conditions,such as small-vessel vasculitides, ulcerative colitis, primarysclerosing cholangitis, and autoimmune hepatitis [2, 3]. Lessfrequently, ANCA induction can occur due to infectionssuch as amebiasis, endocarditis, tuberculosis,malaria, humanimmunodeficiency virus infection, and hepatitis C virus(HCV) infection [2, 4]. Because autoimmune and infectiousdiseases may present similarly, ANCA positivity must becarefully interpreted [5]. The following case describes a 43-year-old male with chronically untreated HCV infection whowas admitted to hospital with infective endocarditis andwas found to be c-ANCA positive. We also summarize theliterature concerning ANCA positivity in endocarditis andHCV infections.

2. Clinical Vignette

A 43-year-old male with a history of HCV infection(untreated since his diagnosis six years previously, with anRNAviral load of 1584 IU/mL on admission) and intravenouspolysubstance use presented to a medical center with acutefever, dyspnea, and arthralgia. He was found to have purpuraover his edematous lower extremities. His initial laboratoryinvestigations featured an elevated white blood cell count of16 × 109 cells per liter, elevated C-reactive protein of 183mg/L,urinalysis that was positive for hematuria, and blood culturesthat were later positive for methicillin-sensitive Staphylococ-cus aureus. He did feature transient acute kidney injury soonafter admission (peak serum creatinine 283 umol/L). Hisserologywas alsopositive for c-ANCA (anti-PR3), antinuclearantibody, and weakly positive for type III cryoglobulinemia.An echocardiogram revealed 1.1 × 1.3 cm tricuspid vegetationinvolving the anterior and septal leaflets. A computerizedtomography scan of his chest illustrated multiple bilateralseptic pulmonary emboli, bilateral pleural effusions, and ananterior mediastinal abscess. A punch biopsy of a purpuric

Hindawi Publishing CorporationCanadian Journal of Infectious Diseases and Medical MicrobiologyVolume 2016, Article ID 3585860, 6 pageshttp://dx.doi.org/10.1155/2016/3585860

2 Canadian Journal of Infectious Diseases and Medical Microbiology

lesion on his right shin, performed one week into antibiotictherapy as his purpura was resolving (Figure 1(a)), revealedmild perivascular inflammation with focally extravasatederythrocytes and hemosiderin deposits consistent with amild or resolving purpuric process (Figure 1(b)). The patientdemonstrated clinical improvement during a six-week courseof cefazolin.

3. Discussion

ANCA positivity may pose a diagnostic and therapeuticquandary in the face of patient presentation consistent witheither a vasculitic or infectious process, particularly in thecase of infective endocarditis [6].

A literature search of previously published cases concern-ingANCA induction in infective endocarditis was performedvia PubMed and Medline using the title and abstract entries“endocarditis” and “ANCA or antineutrophil cytoplasmicantibody,” yielding 70 relevant cases [1, 5–39]. A recent publi-cation by Ying et al. (2014) describes 13 of these cases in addi-tion to a literature review of several other ones [7]. We haveexpanded on this review through the addition of 26 othercases (Table 1).

A set of diagnostic aids between infective endocarditisand small-vessel vasculitis has been previously outlined(Table 2) [8]. One similarity, for example, is acute renalfailure, the prevalence of which in bacterial endocarditis is30% and is a significant predictor ofmortality [40]. Glomeru-lonephritis in infective endocarditis is either pauci-immune,postinfective, or subendothelial membranoproliferative [41],the etiology of which can usually be discerned by obtaining akidney biopsy [8].

Another ANCA-associated infection present in ourreported patient is HCV infection. Previously published casesof ANCA induction due to hepatitis C infection are alsosummarized (Table 3) [6, 9, 42–54]. Our case report hencefeatures two possible infections for c-ANCA induction, bothofwhich likely also contributed to the patient’s cryoglobuline-mia. Because ANCA induction is more common in chronicinfections [6], it argues for hepatitis C as the cause of thispatient’s ANCApositivity as opposed to themore acute infec-tion Staphylococcus aureus endocarditis [55]. Had his ANCAstatus been checked after endocarditis recovery, ANCAinduction due to endocarditis as opposed to hepatitis Cwouldhave also been supported by a normalized or negative ANCAtiter [11].

4. Conclusion

In light of its use in the diagnostic evaluation of vasculitis, apositive ANCA may allow for an infection to mislead a diag-nostician down the path of autoimmune possibilities, partic-ularly in the context of infective endocarditis. While cluesmay be drawn from clinical, laboratory, and radiological datato help differentiate infective endocarditis from vasculitis,obtaining blood cultures is of foremost importance. Makingsuch a distinction will avoid the detrimental consequence ofinitiating immunosuppressive therapy against an infectionmasquerading as an inflammatory disease.

Table 1: Number of positive clinical and laboratory characteristicsamong all previously reported cases of ANCA-positive infectiveendocarditis∗.

Patient characteristicProportion among70 reported patient

casesMean age (years) 53.2Male/female 54/16Valve involvement 56/70Aortic 22Mitral 16Left-sided not otherwise specified 7Aortic plus mitral 6Tricuspid 5Pulmonary 1Mitral plus pulmonary and tricuspid 1Ventricular septal defect 1

Clinical featuresFever 46Anemia 34Splenomegaly 19Nephropathy (GN or AKI) 43Arthralgia 17Lower extremity edema 23Rash 15Purpura 11Cerebral infarction 7Finger clubbing 4

Laboratory resultsPR3 52MPO 8PR3 + MPO 7Hematuria 49Proteinuria 14

MicrobiologyPositive blood culture 54/70PathogenStreptococcus spp. 28Enterococcus spp. 7Staphylococcus spp. 10Bartonella spp. 9Neisseria spp. 1Propionibacterium spp. 1Haemophilus spp. 1Gemella spp. 1Aggregatibacter spp. 1

GN: glomerulonephritis; AKI: acute kidney injury; PR3: proteinase 3; MPO:myeloperoxidase; spp.: species.∗This table, taken fromYing et al. (2014)with permission, expands the reviewfrom the original 44 patients to include 26 others [7].

Canadian Journal of Infectious Diseases and Medical Microbiology 3

Table 2: Diagnostic aids for differentiating between infectious endocarditis and small-vessel vasculitis∗.

Similaritiesa Differencesb

(i) Presentation withconstitutional symptoms (i) Splenomegaly

(ii) Pyrexia (ii) Thrombocytopenia(iii) Active urinarysediment (iii) Hypocomplementemia

(iv) Skin involvement (iv) Immune complexes(v) Decreased GFR (v) Other positive autoantibodies(vi) Increasedinflammatory marker levels (vi) Low titer ANCA/ELISA negative

(vii) Other organ involvementANCA: antineutrophil cytoplasmic antibody; ELISA: enzyme-linked immunosorbent assay; GFR: glomerular filtration rate.aFeatures seen in both conditions.bFeatures seen predominantly in infectious endocarditis.∗This table was taken from Forbes et al. (2012) with permission [8].

Table 3: Summary of previously published ANCA-positive hepatitis C infection cases.

Paper Age (years),sex ANCA Miscellaneous features

Bonaci-Nikolic etal., 2010 [6]

63, F MPO —51, F MPO —24, F MPO —

Cojocaru et al., 2007[42] Mean 75 21 PR3 Concomitant ischemic stroke

Cojocaru et al., 2006[43] ? ? —

Gatselis et al., 2006[44] ? 65 c-ANCA, 4 p-ANCA (though all negative

for PR3 and MPO)

Lamprecht et al.,2003 [9]

?

6 bactericidal/permeability-increasing proteinsMixed cryoglobulinemia4 cathepsin G proteins

1 unknown antigen (c-ANCA)2 bactericidal/permeability-increasing proteins No cryoglobulinemiaFour patients: cathepsin G

Zandman-Goddardet al., 2003 [45] 34, M c-ANCA and p-ANCA Complicated by transverse myelitis

Tajima et al., 2002[46] 66, F p-ANCA Complicated by pachymeningitis

Wu et al., 2002 [47] ? 253 PR3,25 PR3 and MPO

Higher proportion of ANCA-positive comparedto ANCA-negative patients with high alanineaminotransferase, high alpha-fetoprotein, skindisease, cirrhosis, and anemia

Agarwal et al., 2001[48] ? 5 p-ANCA —

Igaki et al., 2000 [49] 60, F MPO Glomerulonephritis, cryoglobulinemiaLamprecht et al.,1998 [50] 60, F c-ANCA Type II cryoglobulinemia

Ohira et al., 1998 [51] ? 12 c-ANCA or p-ANCA —Kallinowski et al.,1997 [52] ? 5 ANCA —

Papi et al., 1997 [53] 63, F MPO Mixed type II cryoglobulinemia, leukocytoclasticvasculitis on skin biopsy

Dalekos andTsianos, 1994 [54] ? 3 ANCA —

F: female; ANCA: antineutrophil cytoplasmic antibody; MPO: myeloperoxidase; PR3: proteinase 3.

4 Canadian Journal of Infectious Diseases and Medical Microbiology

(a) (b)

Figure 1: (a) Photograph of the patient’s resolving purpura involving his legs oneweek into antibiotic therapy. (b) Corresponding hematoxylinand eosin-stained histopathology at 20x magnification of a punch biopsy of one of the lesions on his leg, showing mild perivascularinflammation with focally extravasated erythrocytes consistent with a resolving purpuric process. No leukocytoclastic vasculitis was seen.

Competing Interests

There are no competing interests to disclose between bothauthors.

Acknowledgments

The authors recognize the pathologist Dr. Karen Naert (Foot-hills Medical Centre, Calgary, Alberta, Canada) as a contrib-utor to this paper for her analysis of the pathology specimenand for supplying the histology image (Figure 1(b)).

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